Home About us Contact
|
Home About us Contact | ||
|
|
||
Electrical Activation (electrical + activation)
Selected AbstractsRelationship Between Regional Shortening and Asynchronous Electrical Activation in a Three-Dimensional Model of Ventricular ElectromechanicsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003TARAS P. USYK Ph.D. Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three-dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as ,50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free-wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end-diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three-dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196-S202, October 2003, Suppl.) [source] Electrical activation of the orbicularis oculi muscle does not increase the effectiveness of botulinum toxin type A in patients with blepharospasmEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2010A. Conte Background:, Our primary aim in this study was to determine whether electrically induced activation of the injected muscle increases effectiveness of botulinum type A toxin (BonT-A) in patients with blepharospasm (BPS). The second aim was to assess the safety of BonT-A by investigating whether BonT-A injection alters the excitability of blink reflex circuits in the brainstem. Methods:, Twenty-three patients with BPS received BonT-A (Botox) injected bilaterally into the orbicularis oculi muscle at a standard dose. In 18 patients, electrically induced muscle activation of the orbicularis oculi muscle on one side was performed for 60 min (4 Hz frequency) in a single session, immediately after BonT-A injection and in five patients for 60 min once a day for five consecutive days. The severity of BPS was assessed clinically with the BPS score. Compound muscle action potential (cMAPs) from the orbicularis oculi muscles were measured bilaterally. The blink reflex recovery cycle was studied at interstimulus intervals of 250 and 500 ms. Participants underwent clinical and neurophysiological assessment before BonT-A injection (T0) and 2 weeks thereafter (T1). Results:, Compound muscle action potential amplitude significantly decreased at T1 but did not differ between stimulated and non-stimulated orbicularis oculi in the two groups. BonT-A injection left the blink reflex recovery cycle tested on the stimulated and non-stimulated sides unchanged. Conclusions:, In patients with BPS, the electrically induced muscle activation neither increases the effectiveness of BonT-A nor produces larger electrophysiological peripheral effects. The lack of BonT-A-induced changes in the blink reflex recovery cycle provides evidence that BonT-A therapy is safe in patients with BPS. [source] Electrical activation of common bile duct nerves modulates sphincter of Oddi motility in the Australian possumHPB, Issue 4 2005Y. Sonoda Abstract Background: Sphincter of Oddi (SO) motility is regulated by extrinsic and intrinsic nerves. The existence of neural circuits between the SO and the proximal extrahepatic biliary tree has been reported, but they are poorly understood. Using electrical field stimulation (EFS), we determined if a neural circuit exists between the common bile duct (CBD) and the SO in anaesthetized Australian brush-tailed possums. Methods: The gallbladder, cystic duct or CBD were subjected to EFS with a stimulating electrode. Spontaneous SO phasic waves were measured by manometry. Results: EFS at sites on the distal CBD (12,20 mm proximal to the SO), but less commonly at more proximal CBD, evoked a variety of responses consisting of an excitatory and/or inhibitory phase. Bi-phasic responses consisting of an excitation followed by inhibition were the most common. Tri-phasic responses were also observed as well as excitation or inhibition only. These evoked responses were blocked by topical application of local anaesthetic to the distal CBD or transection of the CBD. EFS at sites on the gallbladder body, neck or cystic duct did not consistently evoke an SO response. Pretreatment with atropine or guanethidine reduced the magnitude of the evoked response by about 50% (p<0.05), pretreatment with hexamethonium had no consistent effect and pretreatment with a nitric oxide synthase inhibitor increased the response. Discussion: A neural circuit(s) between the SO and the distal CBD modulates SO motility. Damage to this area of the CBD during bile duct exploration surgery could adversely affect SO motility. [source] Vasopressin Regulation of Noradrenaline Release Within the Supraoptic NucleusJOURNAL OF NEUROENDOCRINOLOGY, Issue 6 2000M. Ludwig The effect of electrically evoked dendritic vasopressin release on noradrenaline release into the hypothalamic supraoptic nucleus was assessed by in vivo microdialysis in conjunction with high pressure liquid chromatography and electrochemical detection. Electrical activation of magnocellular supraoptic neurones by stimulation of their axons at the level of the neural lobe significantly increased noradrenaline release into the nucleus (2.5-fold, P<0.03). This increase was completely blocked by administration of a nonpeptide vasopressin V1a receptor antagonist via the microdialysis probe. These data suggest that dendritically released vasopressin facilitates noradrenaline release into the hypothalamic nucleus. [source] Inhibition of superior colliculus neurons by a GABAergic input from the pretectal nuclear complex in the ratEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2004Gesche Born Abstract The mammalian pretectal nuclear complex (PNC) is a visual and visuomotor control structure which is strongly connected to other subcortical visual structures. This indicates that the PNC also controls subcortical visual information flow during the execution of various oculomotor programs. A prominent, presumably GABAergic, projection from the PNC targets the superficial grey layer of the superior colliculus (SC), which itself is a central structure for visual information processing necessary for the generation of saccadic eye movements. In order to characterize the pretecto-tectal projection in vitro, we performed whole-cell patch-clamp recordings from SC and PNC neurons in slices obtained from 3,6-week-old pigmented rats. Focal glutamate injections into the PNC and electrical PNC stimulation were used to induce postsynaptic responses in SC neurons. Electrical stimulation of the SC allowed electrophysiological identification of PNC neurons that provide the inhibitory pretecto-tectal input. Only inhibitory postsynaptic currents could be elicited in SC neurons both by pharmacological and by electrical activation of the ipsilateral PNC. Concomitantly, a small number of PNC neurons could be antidromically activated from the ipsilateral SC. Most SC cells postsynaptic to the prectectal input showed the dendritic morphology of wide-field and narrow-field cells and are therefore regarded as projection neurons. All inhibitory currents evoked by PNC activation could be completely blocked by bath application of the selective GABAA receptor antagonist bicuculline. Together these results indicate that SC projection neurons receive a direct inhibitory input from the ipsilateral PNC and that this input is mediated by GABAA receptors. [source] A Tissue-Specific Model of Reentry in the Right Atrial AppendageJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2009JICHAO ZHAO Ph.D. Introduction: Atrial fibrillation is prevalent in the elderly and contributes to mortality in congestive heart failure. Development of computer models of atrial electrical activation that incorporate realistic structures provides a means of investigating the mechanisms that initiate and maintain reentrant atrial arrhythmia. As a step toward this, we have developed a model of the right atrial appendage (RAA) including detailed geometry of the pectinate muscles (PM) and crista terminalis (CT) with high spatial resolution, as well as complete fiber architecture. Methods and Results: Detailed structural images of a pig RAA were acquired using a semiautomated extended-volume imaging system. The generally accepted anisotropic ratio of 10:1 was adopted in the computer model. To deal with the regional action potential duration heterogeneity in the RAA, a Courtemanche cell model and a Luo-Rudy cell model were used for the CT and PM, respectively. Activation through the CT and PM network was adequately reproduced with acceptable accuracy using reduced-order computer models. Using a train of reducing cycle length stimuli applied to a CT/PM junction, we observed functional block both parallel with and perpendicular to the axis of the CT. Conclusion: With stimulation from the CT at the junction of a PM, we conclude: (a) that conduction block within the CT is due to a reduced safety factor; and (b) that unidirectional block and reentry within the CT is due to its high anisotropy. Regional differences in effective refractive period do not explain the observed conduction block. [source] Mapping of Epicardial Activation in a Rabbit Model of Chronic Myocardial Infarction:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007Endocardial, Epicardial Pacing, Response to Atrial Introduction: This study examines the consequences of a large transmural apical infarct on the epicardial electrical activity in isolated rabbit hearts. Methods and Results: Hearts were isolated 8 weeks after coronary artery ligation. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was ,20% of those in the noninfarcted zone (NZ). Epicardial activation mapping of the LV free wall showed that during right atrial (RA) pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. However, direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV ,5 cm/s,1, ,10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was ,50% of normal. A prominent endocardial rim of myocardium in the infarct was not the source of epicardial optical signals because chemical ablation of the endocardium did not affect the epicardial activation pattern. Concluson: Therefore, remnant groups of myocytes in the mid-wall and epicardium of the infarct scar support normal electrical activation during RA pacing. Areas of delayed conduction emerge only on epicardial stimulation. [source] Biventricular Pacing and Left Ventricular Pacing in Heart Failure:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2004Similar Hemodynamic Improvement Despite Marked Electromechanical Differences Introduction: We conducted an acute echocardiographic study comparing hemodynamic and ventricular dyssynchrony parameters during left ventricular pacing (LVP) and biventricular pacing (BVP). We sought to clarify the mechanisms responsible for similar hemodynamic improvement despite differences in electrical activation. Methods and Results: Thirty-three patients underwent echocardiography prior to implantation with a multisite pacing device (spontaneous rhythm [SR]) and 2 days after implantation (BVP and LVP). Interventricular dyssynchrony (pulsed-wave Doppler), extent of myocardium displaying delayed longitudinal contraction (%DLC; tissue tracking), and index of LV dyssynchrony (pulsed-wave tissue Doppler imaging) were assessed. Compared to SR, BVP and LVP caused similar significant improvement of cardiac output (LVP: 3.2 ± 0.5, BVP: 3.1 ± 0.7, SR: 2.3 ± 0.6 L/min; P < 0.01) and mitral regurgitation (LVP: 25.1 ± 10, BVP: 24.7 ± 11, baseline: 37.9 ± 14% jet area/left atria area; P < 0.01). LVP resulted in a smaller index of LV dyssynchrony than BVP (29 ± 10 vs 34 ± 14; P < 0.05). However, LVP exhibited a longer aortic preejection delay (220 ± 34 vs 186 ± 28 msec; P < 0.01), longer LV electromechanical delays (244.5 ± 39 vs 209.5 ± 47 msec; P < 0.05), greater interventricular dyssynchrony (56.6 ± 18 vs 31.4 ± 18; P < 0.01), and higher%DLC (40.1 ± 08 vs 30.3 ± 09; P < 0.05), leading to shorter LV filling time (387 ± 54 vs 348 ± 44 msec; P < 0.05) compared to BVP. Conclusion: Although LVP and BVP provide similar hemodynamic improvement, LVP results in more homogeneous but substantially delayed LV contraction, leading to shortened filling time and less reduction in postsystolic contraction. These data may influence the choice of individual optimal pacing configuration. [source] Relationship Between Regional Shortening and Asynchronous Electrical Activation in a Three-Dimensional Model of Ventricular ElectromechanicsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003TARAS P. USYK Ph.D. Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three-dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as ,50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free-wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end-diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three-dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196-S202, October 2003, Suppl.) [source] Human submucosal neurones regulate intestinal epithelial cell proliferation: evidence from a novel co-culture modelNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2003F. Toumi Abstract The role of the human enteric nervous system (ENS) in the control of the intestinal epithelium organization and proliferation is unknown. To address this issue, we developed a novel co-culture model, consisting of human submucosa containing the submucosal plexus and a human colonic epithelial monolayer. After 3 days in basal conditions (i.e. in absence of neuronal activation) epithelium disorganization and proliferation occurred. In contrast, electrical activation of submucosal neurones maintained monolayer organization and decreased cell proliferation. These effects were blocked by tetrodotoxin and a vasoactive intestinal peptide (VIP) receptor antagonist, and reproduced by VIP. In conclusion, our study suggests that the human ENS is involved in the control of epithelial cell proliferation. [source] Pudendal nerve stimulation evokes reflex bladder contractions in persons with chronic spinal cord injury,,NEUROUROLOGY AND URODYNAMICS, Issue 7 2007Paul B. Yoo Abstract Aims Although electrical stimulation of the pudendal nerve has been shown to evoke reflex micturition-like bladder contractions in both intact and spinalized cats, there is little evidence to suggest that an analogous excitatory reflex exists in humans, particularly those with spinal cord injury (SCI). We present two cases where electrical activation of pudendal nerve afferents was used to evoke excitatory bladder responses. Subjects and Methods A percutaneously placed catheter electrode was used to electrically stimulate the pudendal nerve trunk in two males with SCI. The response was quantified with recorded changes in detrusor pressure and EMG activity of the external anal sphincter. Results In both individuals, frequency specific (f,=,20,50 Hz) activation of the pudendal nerve trunk evoked excitatory bladder contractions that also depended on the stimulus amplitude and bladder volume. Conclusion The results suggest that selective activation of the perineal branches of the pudendal nerve may further augment the excitatory reflex evoked by electrical stimulation. Neurourol. Urodynam. 26:1020,1023, 2007. © 2007 Wiley-Liss, Inc. [source] Effect of Right Ventricular Apex Pacing on the Tei Index and Brain Natriuretic Peptide in Patients with a Dual-Chamber PacemakerPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2006HITOSHI ICHIKI Background: Asynchronous electrical activation induced by right ventricular apex (RVA) pacing can cause various abnormalities in left ventricular (LV) function, particularly in the context of severe LV dysfunction or structural heart disease. However, the effect of RVA pacing in patients with normal LV and right ventricular (RV) function has not been fully elucidated. The aim of this study was to characterize the effects of RVA pacing on LV and RV function by assessing isovolumic contraction time and isovolumic relaxation time divided by ejection time (Tei index) and by assessing changes in plasma brain natriuretic peptide (BNP). Methods: Doppler echocardiographic study and BNP measurements were performed at follow-up (mean intervals from pacemaker implantation, 44 ± 75 months) in 76 patients with dual chamber pacemakers (sick sinus syndrome, n = 30; atrioventricular block, n = 46) without structural heart disease. Patients were classified based on frequency of RVA pacing, as determined by 24-hour ambulatory electrocardiogram (ECG) that was recorded just before echocardiographic study: pacing group, n = 46 patients with RVA pacing ,50% of the time, percentage of ventricular paced 100 ± 2%; sensing group, n = 30, patients with RVA pacing <50% of the time, percentage of ventricular paced 3 ± 6%. Results: There was no significant difference in mean heart rate derived from 24-hour ambulatory ECG recordings when comparing the two groups (66 ± 11 bpm vs 69 ± 8 bpm). LV Tei index was significantly higher in pacing group than in sensing group (0.67 ± 0.17 vs 0.45 ± 0.09, P < 0.0001), and the RV Tei index was significantly higher in pacing group than in sensing group (0.34 ± 0.19 vs 0.25 ± 0.09, P = 0.011). Furthermore, BNP levels were significantly higher in pacing group than in sensing group (40 ± 47 pg/mL vs 18 ± 11 pg/mL, P = 0.017). With the exception of LV diastolic dimension (49 ± 5 mm vs 45 ± 5 mm, P = 0.012), there were no significant differences in other echocardiographic parameters, including left atrium (LA) diameter (35 ± 8 mm vs 34 ±5 mm), LA volume (51 ± 27 cm3 vs 40 ± 21 cm3), LV systolic dimension (30 ± 6 mm vs 29 ± 7 mm), or ejection fraction (66 ± 9% vs 63 ± 11%), when comparing the two groups. Conclusions: These findings suggest that the increase of LV and RV Tei index, LVDd, and BNP are highly correlated with the frequency of the RVA pacing in patients with dual chamber pacemakers. [source] Relation Between the Pacing Induced Sequence of Activation and Left Ventricular Pump Function in AnimalsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2002FRITS W. PRINZEN PRINZEN, F.W., et al.: Relation Between the Pacing Induced Sequence of Activation and Left Ventricu-lar Pump Function in Animals. The main goal of this article was to review animal experimental work on the effect of asynchronous activation on ventricular pump function. During normal sinus rhythm and atrial pacing, the Purkinje system contributes significantly to the rapid electrical activation of the ventricles. In contrast, during ventricular pacing the impulse is almost exclusively conducted through the normal myocardium. As a consequence, electrical activation of the ventricles becomes asynchronous and has an abnormal sequence. The abnormal impulse conduction causes considerable disturbances to occur in regional systolic fiber shortening, mechanical work, blood flow, and oxygen consumption; low values occurring in early activated regions and values above normal being present in late activated regions. Many animal studies have now shown that the abnormal electrical activation, induced by ventricular pacing, leads to a depression of systolic and diastolic LV function. Pacing at the right ventricular apex (the conventional pacing site) reduces LV function more than pacing at the high ventricular septum or at LV sites. In canine hearts with experimental LBBB, LV pacing significantly improves LV pump function. Differences in LV pump function between (combinations of) pacing sites are poorly correlated with QRS duration. Therefore, the cause of the depression of LV function during abnormal electrical activation appears to be a combination of the asynchrony and the sequence of activation. These experimental findings justify continuing attention for optimizing the site(s) of ventricular pacing in patients with normal and abnormal ventricular impulse conduction. [source] Effects of Gonadotropins on In Vitro Maturation and of Electrical Stimulation on Parthenogenesis of Canine OocytesREPRODUCTION IN DOMESTIC ANIMALS, Issue 1 2010BS Kim Contents The objective of this study was to determine the effects of gonadotropins on in vitro maturation (IVM) and electrical stimulation on the parthenogenesis of canine oocytes. In experiment I, cumulus oocyte complexes were collected from ovaries at a random phase of the oestrus cycle and cultured on maturation medium treated with hCG or eCG for 48 or 72 h. There were no significant differences in the effects on the metaphase II (MII) rate between the hCG and eCG treatment groups over 48 h (5.4% vs 5.5%). The MII rate in the co-treatment group of hCG and eCG for 48 h was higher than in each hormone treated group (15.5%, p < 0.05). In experiment 2, the parthenogenetic effect on oocyte development, at various electrical field strengths (1.0, 1.5, 2.0 kV/cm DC) for 60 or 80 ,s with a single DC pulse after IVM on the co-treatment of hCG and eCG, was examined. The rate of pronuclear formation (37.1%) in electrical activation at 1.5 kV/60 ,s without cytochalasin B (CB) was higher than that of oocytes activated in the other groups (p < 0.05). However, we did not observe the cleavage stages. Also, CB did not influence parthenogenesis of canine oocytes. The results showed that the pronucleus formation rate, indicative of the parthenogenesis start point, could be increased by electrical stimulation. Therefore, these results can provide important data for the parthenogenesis of canine oocytes and suggest the probability of parthenogenesis in canines. [source] Neurotrophic effects of GM1 ganglioside and electrical stimulation on cochlear spiral ganglion neurons in cats deafened as neonatesTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 6 2007Patricia A. Leake Abstract Previous studies have shown that electrical stimulation of the cochlea by a cochlear implant promotes increased survival of spiral ganglion (SG) neurons in animals deafened early in life (Leake et al. [1999] J Comp Neurol 412:543,562). However, electrical stimulation only partially prevents SG degeneration after deafening and other neurotrophic agents that may be used along with an implant are of great interest. GM1 ganglioside is a glycosphingolipid that has been reported to be beneficial in treating stroke, spinal cord injuries, and Alzheimer's disease. GM1 activates trkB signaling and potentiates neurotrophins, and exogenous administration of GM1 has been shown to reduce SG degeneration after hearing loss. In the present study, animals were deafened as neonates and received daily injections of GM1, beginning either at birth or after animals were deafened and continuing until the time of cochlear implantation. GM1-treated and deafened control groups were examined at 7,8 weeks of age; additional GM1 and no-GM1 deafened control groups received a cochlear implant at 7,8 weeks of age and at least 6 months of unilateral electrical stimulation. Electrical stimulation elicited a significant trophic effect in both the GM1 group and the no-GM1 group as compared to the contralateral, nonstimulated ears. The results also demonstrated a modest initial improvement in SG density with GM1 treatment, which was maintained by and additive with the trophic effect of subsequent electrical stimulation. However, in the deafened ears contralateral to the implant SG soma size was severely reduced several months after withdrawal of GM1 in the absence of electrical activation. J. Comp. Neurol. 501:837,853, 2007. © 2007 Wiley-Liss, Inc. [source] Ionic Mechanisms and Vectorial Model of Early Repolarization Pattern in the Surface Electrocardiogram of the AthleteANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2008Eduardo C. Barbosa M.D. Background: The electrocardiogram (ECG) of the athlete displays particular characteristics as a consequence of both electrophysiological and autonomic remodeling of the heart that follows continued physical training. However, doubts persist on how these changes directly interact during ventricular activation and repolarization ultimately affecting surface ECG waveforms in athletes. Objective: This article considers an in deep rationale for the electrocardiographic pattern known as early repolarization based on both electrophysiological mechanisms at cellular level and the vectorial theory of the cardiac activation. Methods: The mechanism by which the autonomic remodeling influences the cardiac electrical activation is reviewed and an insight model of the ventricular repolarization based on ionic models and the vectorial theory of the cardiac activation is proposed. Results: Considering the underlying processes related to ventricular electrical remodeling, we propose that, in athletes' heart: 1) vagal modulation increases regional electrophysiological differences in action potential phases 1 and 2 amplitudes, thus enhancing a voltage gradient between epicardial and endocardial fibers; 2) this gradient affects depolarization and repolarization timing sequences; 3) repolarization wave front starts earlier on ventricular wall and partially overcomes the end of depolarization causing an upward displacement of the J-point, ST segment elevation, and inscription of magnified T-waves amplitudes leading to characteristic surface ECG waveform patterns. Conclusions: In athletes, the association between epicardial to endocardial electrophysiological differences and early repolarization ECG pattern can be demonstrated by the vectorial theory of the ventricular activation and repolarization. [source] Modulation of gap junctions by nitric oxide contributes to the anti-arrhythmic effect of sodium nitroprusside?BRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2009Márton Gönczi Background and purpose:, Nitric oxide (NO) donors provide a preconditioning-like anti-arrhythmic protection in the anaesthetized dog. As NO may modulate gap junction (GJ) function, the present study investigated whether this anti-arrhythmic effect is due to a modification of GJs by NO, derived from the NO donor sodium nitroprusside (SNP). Experimental approach:, In chloralose-urethane-anaesthetized, open-chest dogs, either saline (controls; n= 11) or SNP (0.2 µg·kg,1·min,1; n= 10) was infused at a rate of 0.5 mL·min,1 by the intracoronary route. The infusions were started 20 min prior to and maintained throughout the entire 60 min occlusion period of the left anterior descending coronary artery. The severity of ischaemia and of arrhythmias, tissue electrical impedance and permeability, as well as the phosphorylation of connexin43, were assessed. Key results:, Compared with the controls, SNP infusion markedly suppressed the total number of ventricular premature beats (666 ± 202 vs. 49 ± 18; P < 0.05), and the number of ventricular tachycardiac episodes (8.1 ± 2.3 vs. 0.2 ± 0.1; P < 0.05) without significantly modifying the incidence of ventricular tachycardia or ventricular fibrillation. The severity of ischaemia (epicardial ST-segment changes, inhomogeneity of electrical activation) and tissue electrical impedance changes were significantly less in the SNP-treated dogs. SNP improved GJ permeability and preserved the phosphorylated form of connexin43. Conclusion and implications:, The anti-arrhythmic protection resulting from SNP infusion in the anaesthethized dog may, in part, be associated with the modulation of gap junctional function by NO. [source] | |||||||||||||